Our working hypothesis is that impulses, originating from the amygdalo-insular networks can drive the behavior through explicit knowledge involving prefrontal and orbitofrontal loops or implicit mechanisms that instead depend upon the functional relationships of these structures with several domains of the striatum.

We suggest that inter-individual vulnerability to develop impulsive/compulsive neuropsychiatric disorders stem from aberrant plasticity processes within the corticostriatal networks governing the translation of impulses into actions that ultimately result in a so-called abnormal incentive habit process.